Reference

Teratogen metabolism: activation of thalidomide and thalidomide analogs to products that inhibit the attachment of cells to concanavalin A coated plastic surfaces

Teratogen metabolism: activation of thalidomide and thalidomide analogs to products that inhibit the attachment of cells to concanavalin A coated plastic surfaces. Braun, Andrew G.; Weinreb, Steven L. (Dep. Radiat. Ther., Harvard Med. Sch., Boston, MA 02115, USA). Biochem. Pharmacol., 33(9), 1471-7 (English) 1984. CODEN: BCPCA6. ISSN: 0006-2952. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Thalidomide (I) [50-35-1] metabolites inhibited the attachment of tumor cells to concanavalin A [11028-71-0]-coated polyethylene surfaces. I, itself, was noninhibitory. I activation to inhibitory products required hepatic microsomes, an NADPH-generating system, and O. Prodn. of inhibitory metabolites was unaffected by either epoxide hydrolase or 1,2-epoxy-3,3,3-trichloropropane, an inhibitor of epoxide hydrolase endogenous to hepatic S9 fraction. Therefore, the attachment inhibitor was probably not an arene oxide. Inhibition was not accompanied by cytotoxicity, as judged by trypan blue exclusion. Although uninduced hepatic microsomes from mice, rats, and dogs had similar abilities to activate I, microsomes from Aroclor 1254-induced rats were relatively inactive in the system. Inhibitory metabolites were generated from the I analogs EM8 [16477-31-9], EM12 [26581-81-7], EM16 [26581-91-9], EM87 [49785-74-2], EM136 [42472-96-8], EM255 [79458-80-3], E350 [303-31-1], phthalimide [85-41-6], phthalimidophthalimide [4388-29-8], indan [496-11-7], 1-indanone [83-33-0] and 1,3-indandione [606-23-5]. Glutarimide [1121-89-7], glutamic acid [56-86-0], and phthalic acid [88-99-3] did not activate to inhibitory products.

Teratogen metabolism: activation of thalidomide and thalidomide analogs to products that inhibit the attachment of cells to concanavalin A coated plastic surfaces

Teratogen metabolism: activation of thalidomide and thalidomide analogs to products that inhibit the attachment of cells to concanavalin A coated plastic surfaces. Revised version. Weinreb, S. L. (Dep. Radiat. Ther., Harvard Med. Sch., Boston, MA, USA). Report, DOE/ER/60070-T1; Order NO. DE84006118, 32 pp. Avail. NTIS From: Energy Res. Abstr. 1984, 9(8), Abstr. No. 15071 (English) 1982. DOCUMENT TYPE: Report CA Section: 1 (Pharmacology) Thalidomide (I) [50-35-1] metabolites inhibit the attachment of tumor cells to concanavalin A-coated polyethylene surfaces. I itself is noninhibitory. I activation to inhibitory products requires hepatic microsomes, an NADPH generating system and mol. O. Prodn. of inhibitory metabolites is unaffected by either epoxide hydrolase or TCPO, an inhibitor of epoxide hydrolase endogenous to hepatic S9 fraction. Therefore, the attachment inhibitor is probably not an arene oxide. Inhibition is not accompanied by cytotoxicity as judged by trypan blue exclusion. Although uninduced hepatic microsomes from mice, rats, and dogs have similar ability to activate I microsomes from Aroclor 1254 induced rats are relatively inactive in the system. Inhibitory metabolites can be generated from the I analogs EM8 [16477-31-9], EM12 [26581-81-7], EM16 [26581-91-9], EM87 [49785-74-2], EM136 [42472-96-8], EM255 [79458-80-3], E350 [303-31-1], phthalimide [85-41-6] phthalimido-phthalimide [4388-29-8] indan [496-11-7], 1-indanone [83-33-0], and 1,3-indandione [606-23-5]. Glutarimide [1121-89-7], glutamic acid [56-86-0] and phthalic acid [88-99-3] do not activate to inhibitory products.